Scientists have identified a protein that acts like a brake on the nervous system’s ability to repair damaged connections. Blocking AHR helped injured nerve fibers regrow and improved movement and sensation in mice with nerve or spinal cord injuries. The discovery could eventually point toward new treatments designed to shift neurons from simply surviving an injury to actively rebuilding themselves.
Do you ever feel like sometimes you can master a new dance step almost immediately, while other times you struggle to nail it despite repeated practice? This might be due to skill or effort, but also to something less obvious: whether the brain is in a state that allows learning to take hold.
The brain does not learn in isolation from the rest of the body. Signals from internal organs continuously reach the brain through a key part of our nervous system called the vagus nerve. Researchers at Tohoku University specializing in super-network brain physiology have now demonstrated in mice that stimulating this nerve after training can promote lasting motor learning. This study reveals a previously underappreciated way in which body-to-brain signaling may support long-term learning.
The findings were published in iScience on August 25, 2026.
Officials said the technology will give patients advanced surgical capabilities from experienced spine specialists without having to travel outside of the region…
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A new Northwestern Medicine study has identified a previously unknown mechanism by which an enzyme promotes cancer cell proliferation, establishing it as a promising therapeutic target for cancer, according to findings published in Nature Communications.
N-acetyltransferase 10 (NAT10) is a multifunctional enzyme with oncogenic properties and has been associated with multiple types of cancer, including hepatocellular carcinoma—an aggressive type of liver cancer—and acute myeloid leukemia, among others.
NAT10 is known to acetylate, or chemically modify, RNA, but whether this mechanism supports the oncogenic properties of this protein has remained uncertain, said Daniel Arango, Ph.D., assistant professor of pharmacology and a co-corresponding author of the study.
Advances in mitochondrial genome editing have expanded efforts to manipulate mitochondrial DNA and model mitochondrial disease. This Review discusses the development of programmable nucleases and mitochondrial base editors, their applications in disease modelling and therapeutic correction, and the key challenges to clinical translation.
Relying on a urinary catheter is a standard part of medical care for hundreds of thousands of patients each year. Unfortunately, the device carries the risk of catheter-associated urinary tract infections (CAUTIs), for which bacteria are widely recognized as the primary cause. And yet, many patients face a growing threat from another pathogen: a fungus, Candida albicans.
Research published in Proceedings of the National Academy of Sciences by University of Notre Dame associate professors of biological sciences Ana Flores-Mireles and Felipe Santiago-Tirado shows how the fungus works in the bladder, potentially changing the way doctors treat and diagnose CAUTIs.
Cancer cells are proving trickier than we thought, so scientists are getting even trickier to shift the survival odds in our favor. Recent medical research has highlighted a significant issue: cancer cells display plasticity. Some cancer cells can spontaneously revert from a differentiated state to become ‘immature’ and stem-cell-like again, switching their identity to yield more diverse, aggressive, and proliferative tumors.
Cancer stem cells (CSCs) are tumor cells that have the principal properties of self-renewal, clonal tumor initiation capacity and clonal long-term repopulation potential. CSCs reside in niches, which are anatomically distinct regions within the tumor microenvironment. These niches maintain the principle properties of CSCs, preserve their phenotypic plasticity, protect them from the immune system and facilitate their metastatic potential. In this perspective, we focus on the CSC niche and discuss its contribution to tumor initiation and progression. Since CSCs survive many commonly employed cancer therapies, we examine the prospects of targeting the niche components as preferable therapeutic targets.